Effect of Killed PRRSV Vaccine on Gut Microbiota Diversity in Pigs

Viruses. 2022 May 18;14(5):1081. doi: 10.3390/v14051081.

Abstract

Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important pathogens affecting the global swine industry. Vaccination is still a main strategy for PRRSV control; however, host factors associated with vaccine efficacy remain poorly understood. Growing evidence suggests that mucosa-associated microbiomes may play a role in the responses to vaccination. In this study, we investigated the effects of a killed virus vaccine on the gut microbiome diversity in pigs. Fecal microbial communities were longitudinally assessed in three groups of pigs (vaccinated/challenged with PRRSV, unvaccinated/challenged with PRRSV, and unvaccinated/unchallenged) before and after vaccination and after viral challenge. We observed significant interaction effects between viral challenge and vaccination on both taxonomic richness and community diversity of the gut microbiota. While some specific taxonomic alterations appear to be enhanced in vaccinated/challenged pigs, others appeared to be more consistent with the levels in control animals (unvaccinated/unchallenged), indicating that vaccination incompletely protects against viral impacts on the microbiome. The abundances of several microbial taxa were further determined to be correlated with the level of viral load and the amount of PRRSV reactive CD4+ and CD8+ T-cells. This study highlights the potential roles of gut microbiota in the response of pigs to vaccination, which may pave the road for the development of novel strategies to enhance vaccine efficacy.

Keywords: PRRSV killed vaccine; gut microbiota; porcine reproductive and respiratory syndrome virus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD8-Positive T-Lymphocytes
  • Gastrointestinal Microbiome*
  • Porcine Reproductive and Respiratory Syndrome* / prevention & control
  • Porcine respiratory and reproductive syndrome virus*
  • Swine
  • Vaccines, Attenuated
  • Vaccines, Inactivated
  • Viral Vaccines*

Substances

  • Vaccines, Attenuated
  • Vaccines, Inactivated
  • Viral Vaccines

Grants and funding

This project was supported by research startup funds (to Ying Fang and Christopher A. Gaulke) from the University of Illinois at Urbana-Champaign. Fangfeng Yuan was partially supported by Illinois Distinguished Fellowship for graduate students at the University of Illinois.